In pursuit of our goal to advance understanding of the processes of growth regulation in normal hepatocytes, and ultimately how chemical carcinogens disrupt that order during oncogenesis, we previously determined that the fatty acid binding protein (L-FABP) of rat liver cytoplasm: (i) is the principal liver protein target of the hepatic carcinogen, N-2-fluorenylacetamide (2-acetylaminofluorene), early during carcinogenesis in rats; (ii) is elevated during mitosis in normal hepatocytes, and (iii) avidly binds growth stimulatory and inhibitory metabolites of arachidonic acid in vitro. These and other in vitro and animal studies revealed that L-FABP binds numerous ligands of potentially great importance in the regulation of growth of hepatocytes. Therefore, in order to understand whether and how these ligand-L-FABP interactions may actually play regulatory roles inside cells, we recently developed a powerful homologous, zero-background model of transfected rat hepatoma HTC cells in culture. Accordingly, using this model cell system we will investigate the following four classes of important ligands of L-FABP for their specific growth modulating functions within the cells: oxygenated metabolites of linoleic acid, peroxisome proliferators, lysophosphatidic acids, and selenium compounds. Relevance to Health. Our findings and proposals bridge the fields of chemical carcinogenesis and its chemoprevention, the actions of liver fatty acid binding protein in normal liver, and the roles of fatty acids and their metabolites, including the eicosanoids and related lipids, in the modulation of cell growth. Collectively, the investigations promise to advance the present understanding of the regulation of normal hepatocytic growth by bioactive lipids, and ultimately to uncover aspects of the perturbations of this system by chemical carcinogens during cancer causation, and by selenium compounds during cancer chemoprevention.